A 58-year-old man from Delhi presents to the emergency department with acute onset chest pain radiating to the left arm for 2 hours. He has a 15-year history of hypertension and type 2 diabetes mellitus, both poorly controlled. On examination, blood pressure is 165/95 mmHg, heart rate 102/min. ECG shows ST elevation in leads II, III, and aVF. Coronary angiography reveals a thrombotic occlusion of the right coronary artery with atherosclerotic plaque. Which of the following histological features is most characteristic of the atherosclerotic plaque that precipitated this acute coronary syndrome?

Explanation

## Pathological Features of Vulnerable Atherosclerotic Plaques ### Histology of Plaque Prone to Rupture **Key Point:** Acute coronary syndromes are typically triggered by rupture of a **vulnerable (unstable) plaque**, not a stable, calcified one. The characteristic features of such plaques are: 1. **Lipid-rich necrotic core** — composed of cholesterol, cholesterol esters, and cellular debris 2. **Thin fibrous cap** — often <65 μm thick, composed of smooth muscle cells and collagen 3. **Abundant inflammatory infiltrate** — macrophage-derived foam cells, T lymphocytes, and mast cells 4. **Neovascularization** — immature vessels prone to hemorrhage 5. **Reduced smooth muscle cells** — due to apoptosis and loss of structural support ### Why This Plaque Type Causes ACS The thin fibrous cap is mechanically weak and prone to rupture under hemodynamic stress (especially in hypertensive patients). Rupture exposes the thrombogenic lipid core to blood, triggering platelet aggregation and thrombus formation — leading to acute occlusion and myocardial infarction. **High-Yield:** The **lipid-rich, thin-capped plaque with foam cells** is the **hallmark of vulnerable plaque** and is the morphological substrate of acute coronary syndromes. This is tested frequently in NEET PG pathology. ### Comparison: Stable vs. Vulnerable Plaques | Feature | Stable Plaque | Vulnerable Plaque | |---------|---------------|-------------------| | Fibrous cap | Thick (>65 μm) | Thin (<65 μm) | | Lipid core | Small, sparse | Large, lipid-rich | | Foam cells | Few | Abundant | | Smooth muscle | Prominent | Sparse/apoptotic | | Calcification | Extensive | Minimal | | Risk of rupture | Low | High | | Clinical presentation | Stable angina | ACS (MI, unstable angina) | **Clinical Pearl:** In this patient, the combination of poorly controlled hypertension and diabetes accelerates atherosclerotic plaque development and destabilization. The acute presentation with ST elevation and angiographic thrombus indicates acute plaque rupture with superimposed thrombosis. **Mnemonic: VULNERABLE PLAQUE = LIPID-RICH, THIN-CAPPED** - **L**ipid-rich necrotic core - **I**nflammatory infiltrate (foam cells, macrophages) - **P**rone to rupture - **I**ntraplaque hemorrhage - **D**ecreased smooth muscle [cite:Robbins 10e Ch 11]